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Frank Review Course > Basic Science Orthobullets/Millers Book > Flashcards

Basic Science Orthobullets/Millers Book Flashcards

1
Q

Overview of anticoagulation

A
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2
Q

What does Aspirin do and how does it work?

A

Introduction:

thromboxane function

under normal conditions thromboxane is responsible for the aggregation of platelets that form blood clots

prostaglandins function prostaglandins are local hormones produced in the body and have diverse effects including

the transmission of pain information to the brain

modulation of the hypothalamic thermostat

inflammation

Mechanism of ASA inhibits the production of prostaglandins and thromboxanes through irreversible inactivation of the cyclooxygenase enzyme within platelets

acts as an acetylating agent where an acetyl group is covalently and irreversibly attached to a serine residue in the active site of the cyclooxygenase enzyme.

this differentiates aspirin different from other NSAIDs which are reversible inhibitors

Metabolism

renal

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3
Q

Unfractionated Heparin (SQ)

A

Mechanism

binds and enhances ability of antithrombin III to inhibit factors IIa, III, Xa

Reversal

protamine sulfate

Metabolism

hepatic

Risk

bleeding

HIT (heparin induced thrombocytopenia)

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4
Q

EnoXAparen

Lovenox

A

Overview

molecular name: enoxaparin

trade name: Lovenox, Clexane

has advantage of not requiring lab value monitoring

Mechanism

LMWH acts in several sites of the coagulation cascade, with its principal action being inhibition of factor Xa

reversed by protamine sulfate

Metabolism

renal

Risk

bleeding

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5
Q

FondaParinux

Arixtra

A

Overview

trade name: Arixtra

has advantage of not requiring lab value monitoring

Mechanism

indirect factor Xa inhibitor (acts through antithrombin III)

Metabolism

renal

Evidence

studies show decreased incidence of DVT when compared to enoxaparin in hip fx and TKA patients

Risk highest bleeding complications

not to be used in conjunction with epidurals

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6
Q

Warfarin

Coumadin

A

Mechanism of anticoagulation inhibits vitamin K 2,3-epoxide reductase

prevents reduction of vitamin K epoxide back to active vitamin K

vitamin K is needed for gamma-carboxylation of glutamic acid for factorsII (prothrombin), VII (first affected), IX, X protein C, protein S

Monitoring

target level of INR (international normalized ratio) is 2-3 for orthopaedic patients

not achieved for 3 days after initiation

Reversal

vitamin K (takes up to 3 days)

fresh frozen plasma (acts immediately)

Risk

difficult to dose requires the frequent need for INR lab monitoring

can have adverse reaction with other drugs including

rifampin

phenobarbital

diuretics

cholestyramine

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7
Q

RIvaroXABAN

XArelto

A

Overview

others in the same class include apixaban (Eliquis) and edoxaban (Savaysa or Lixiana)

mechanism of action of these drugs can be deduced from the name.

Rivaro(Identifier)-xa(FactorXa)-ban(inhibitor)

Mechanism

direct Xa inhibitor

Metabolism

liver

Antidote

no current antidote- why you have to wait with surgery

andexanet alpha being investigated

Risk

bleeding

Half-life

8-hours (12-hours for apixaban)

urgent surgical procedures delayed until half-life spanned from last dose

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8
Q

Diabigatran

Pradaxa

A

Mechanism

reversible direct thrombin (factor IIa) inhibitor

Metabolism

renal

Antidote

idarucizumab (FDA approved Oct 2015)

Risk

GI upset

bleeding

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9
Q

Transexamanic Acid

TXA

synthethic lysine

A

Overview

an antifibrinolytic that promotes and stabilizes clot formation

studies have shown that TXA reduce perioperative blood loss and transfusion in THA and TKA

Mechanism

synthetic derivative of the amino acid lysine

competitively inhibits the activation of plasminogen by binding to the lysine binding site

at high concentrations, is a non-competitive inhibitor of plasmin

has roughly 8-10 times the antifibrinolytic activity of ε-aminocaproic acid

Dosing intravenous

10-20 mg/kg initial bolus dose followed by repeated doses of the initial TXA dose every 3 hours for 1-4 doses

10-20mg initial bolus followed either by an infusion of 1-10 mg/kg/hr for 4-30 hours

topical application is as effective as IV

sprayed onto open wound at completion of procedure

no detectable TXA in the bloodstream after topical application

Metabolism

<5% of the drug is metabolized

biological half-life in joint fluid is 3h, present in tissues for up to 17h

Risks

systematic review shows no increase in thromboembolic events

relatively few adverse reactions have been reported in the arthroplasty literature

**Tranexamic acid (TXA) works through the competitive inhibition of plasminogen activation.

TXA (Lysteda) is an antifibrinolytic that promotes and stabilizes clot formation. It competitively inhibits the activation of plasminogen by binding to the lysine binding site. TXA is effective in reducing the need for blood transfusions while not increasing the risk of VTE and renal complications. However, it is still advised that patients with cardiac stents and previous thromboembolic events including ischemic stroke not be administered TXA.**

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10
Q

Herbal supplements that affect bleeding:

A

Increased bleeding

gingko, ginseng, and garlic have been found to increase the rate of bleeding

related to effect on platelets

proper history taking can avoid complications

Increased warfarin effect (increase INR)omega-3 fish oil

affects platelet aggregation and vitamin K dependent coagulation factors

Reduced warfarin effect (reduces INR)

coenzyme Q10

green tea

direct warfarin antagonist (reduces INR)

St John’s wort

increases catabolism of warfarin (reduces INR)

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11
Q

where do Anticoagulants act on the clotting cascade?

A
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12
Q

what are the criteria vis MSIS for an infected periprosthethic joint?

A
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13
Q

What are the mechanism of actions for heparin, aspirin, warfarin, rivoxaban, dabigatran

the big Atran–

A

Warfarin inhibits vitamin K 2,3-epoxide reductase, thereby limiting the production of vitamin K-dependent clotting factors (II, VII, IX, X) as well as Protein C and Protein S.

Aspirin inhibits the production of prostaglandins and thromboxanes through irreversible inhibition of cyclooxygenase (COX, 1 and 2) and thus inhibits platelet aggregation.

Rivaroxaban is a direct inhibitor of factor Xa.

Dabigatran is a direct thrombin inhibitor.

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14
Q

Describe Transaminic Acid:

A

Factor Ia is fibrin. The enzyme that breaks down fibrin is plasmin. Tranexamic acid (TXA) is an antifibrinolytic that prevents the activation of plasmin from the inactive zymogen plasminogen.

Tranexamic acid competitively inhibits the activation of plasminogen to plasmin by binding to specific sites on both plasminogen and plasmin. Tranexamic acid has roughly eight times the antifibrinolytic activity of an older analogue, e-aminocaproic acid. It is used during joint replacement surgery to reduce blood loss and the need for transfusion.

Watts et al. review strategies for minimizing blood loss and transfusion. They recommend 1g of TXA prior to incision, and 1g at wound closure. They also recommend giving fluids for symptoms of anemia, rather than transfusion, as even high risk patients do well with sufficient intravascular volume even with low hemoglobin levels.

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15
Q

what are the half-lives of anticoagulation medications as it relates to surgery?

A

Warfarin, which is dosed daily, can take 72 to 96 hours to reach therapeutic levels. It has a plasma half-life of 36 to 42 hours. Low-molecular heparins have a plasma half-life of 4 to 5 hours, and fondaparinux has a half-life of 17 to 21 hours. Warfarin will not affect the International Normalized Ratio (INR) until 2 to 3 days after it is given. Patients on chronic warfarin therapy should have treatment stopped 3 to 5 days before elective surgery to allow the INR to normalize.

Xarelto is 8-12 hours. have to hold urgent surgery for those on it.

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16
Q

What herbal supplements affect platelets

A

Ginko

Garlic

Ginseng

The three G’s

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17
Q

what is the clotting cascade’s final product?

A

Thrombin–

converts soluble fibrinogen to insoluable fibrin

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18
Q

Review the genetic components of hypercoagulability:

A
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19
Q

List the risk factors for thromboembolic disease:

A
20
Q

what are the recommendations on preventing VTE on arthroplasty?

A
21
Q

Miller’s brief review of pharmacologic treatment for SVT prophylaxis:

A

Pharmacologic prophylaxis:

Surgical Care Improvement Project (SCIP) quality measures require DVT prophylaxis.

Aspirin

Irreversibly binds and inactivates COX in platelets, thereby reducing thromboxane A2

Weakest: Use of IPCD encouraged

Low bleeding risk: Should be considered for patients at higher risk for bleeding.

•

Warfarin (Coumadin)

Prevents vitamin K γ-carboxylation in liver

Inhibits factors II, VII, IX, X, and proteins C and S

Vitamin K and fresh frozen plasma can reverse

Multiple reactions with drugs and diet

Must be monitored with international normalized ratio (INR; goal, 2–3)

•

Heparin

Activates antithrombin III (ATIII), which then inactivates factor Xa and thrombin

Protamine sulfate can reverse

Short half-life: 2 hours

High bleeding rate in arthroplasty

Binds platelets—heparin-induced thrombocytopenia

Low-molecular-weight heparin (LMWH)

Reversibly inhibits factor Xa through ATIII and factor II

Protamine sulfate can reverse•

No monitoring needed

Less heparin-induced thrombocytopenia

•

Higher risk for bleeding than with warfarin

•

Fondaparinux (akin to oral heparin)

•

Irreversibly but indirectly inhibits factor X through ATIII

Synthetic pentasaccharide

No monitoring

No antidote

Higher risk for bleeding than with LMWH

Rivaroxaban

Direct Xa inhibitor

Oral drug

Higher risk for bleeding than with LMWH

Hirudin

Direct thrombin (IIa) inhibitor

Intramuscular and oral (dabigatran) versions

No antidote

•

Inferior vena cava (IVC) filter use: controversial

Should be considered in following conditions:

Contraindication to prophylaxis

Cerebral bleed/trauma

Spine surgery

Prior complication of prophylaxis

22
Q

How do you assess cardiac risk factors prior to surgery?

A

American College of Cardiology/American Heart Association (ACC/AHA) elements for assessing risk

Clinical risk factors in perioperative cardiac risk

Major predictors

Unstable/severe angina, recent MI (<6 weeks)

Worsening or new-onset CHF

Arrhythmias

Atrioventricular (AV) block

Symptomatic ventricular dysrhythmia: bradycardia (<30 beats/min), tachycardia (>100 beats/min)

Severe aortic stenosis or symptomatic mitral stenosis

Other

Prior ischemic heart disease

Prior CHF

Prior stroke/TIA

Diabetes

Renal insufficiency (creatine >2 mg/dL)

Functional exercise capacity—measured in metabolic equivalents (METs) MET: 3.5 mL O2 uptake/kg/min

Perioperative risk elevated if unable to meet 4-MET demand

Walk up flight of steps or hill (= 4 METs)

Heavy work around house (>4 METs)

Can patient walk four blocks or climb two flights of stairs?

23
Q

Please quantify surgery specific risks by procedure:

A

Surgery-specific risk:

•

High risk (>5% risk of death/MI)

Aortic, major or peripheral vascular procedures

Intermediate risk (1%–5% risk of death/MI)

Orthopaedic, ENT, abdominal/thoracic or procedures

Low risk (<1% risk of death/MI)—usually do not need further clearance

•

Ambulatory surgery, endoscopic or superficial procedures

24
Q

What are cardiac recommendations prior to surgery?

A

Twelve-lead ECG if:

CAD and intermediate-risk procedure

One clinical risk factor and intermediate-risk procedure

Noninvasive evaluation of left ventricular function if:

—Three or more clinical risk factors and intermediate- risk procedure

—Dyspnea of unknown origin

—CHF with worsening dyspnea without testing in 12 months

β-Blockers and statins should be continued around the time of surgery.

Acetylsalicylic acid (ASA) should be stopped 7 days prior to surgery.

Cardiology consultation should be considered for patients taking other agents (clopidogrel, prasugrel).

Risk of stent thrombosis balanced with that of surgical bleed

25
Q

What are measures of shock recovery?

A

Lactate—indirect marker of tissue hypoperfusion

•

Best measures of adequate resuscitation:

Clinical measure of organ function: urine output more than 30 mL/h

Laboratory measure: serum lactate less than 2.5 mg/dL

26
Q

Review the types of shock and their clinical presentation:

A

Neurogenic shock

High spinal cord injury (also anesthetic accidents)

Loss of sympathetic tone and of vasomotor tone of peripheral arterial bed

Bradycardia, hypotension, warm extremities

Treatment: vasoconstrictors and volume

•

Septic shock (vasogenic)

Number one cause of ICU death

Mortality 50%

Bacterial toxins stimulate cytokine storm.

Examples: gram-negative lipopolysaccharides, toxic shock superantigen

Inflammatory mediators cause endothelial dysfunction and peripheral vasodilation

•

Treatment:

Identification and treatment of infections

Prompt resection of dead tissue

Appropriate antibiotics

Cardiogenic shock

Bad pump: Extensive MI, arrhythmias

Blocked pump (obstructive shock)

Massive “saddle” pulmonary embolism

Tension pneumothorax

Cardiac tamponade

Beck triad: hypotension, muffled heart sounds,

neck vein distension

Pulsus paradoxus

Decreased systolic BP with inspiration

Treatment: pericardiocentesis

Hypovolemic shock:

Most common shock of trauma

Volume loss from bleeds or burns

“Third spacing” also a cause

Neuroendocrine response: save heart and brain

Peripheral vasoconstriction

BP may be normal

Pale, cold, clammy extremities

Percentage of blood loss key to symptoms/signs:

Class I: up to 15% blood volume loss

Vital signs can be maintained.

Pulse below 100 beats/min

Class II: 15%–30% blood volume loss

Tachycardia (>100 beats/min), orthostatic,

Anxious

Increased diastolic BP

Class III: 30%–40% blood volume loss

Decreased systolic BP

Oliguria

Confusion, mental status changes

Class IV: more than 40% blood volume loss

Life threatening; patient is obtunded

Narrowed pulse pressure

IImmeasurable diastolic BP

Treatment

First, ABCs of resuscitation: then, bleeding must be stopped.

Blood products make better resuscitation fluids than saline.

27
Q

How to address perioperative pulmonary issues around surgery:

A

Higher in cases that involve thorax such as scoliosis

Highest in patients with prior disease

Spinal/epidural anesthesia favored over general

Medical treatment should be maximized around surgery.

Symptomatic COPD: anticholinergic inhalers (ipratropium; May require corticosteroids

Asthma

Presence of wheezes or shortness of breath: β-agonist inhalers (albuterol)

Perioperative oral steroids safe

Systemic glucocorticoid should be considered if forced expiratory volume in 1 minute (FEV1) or peak expiratory flow rate (PEFR) is below 80% predicted values/personal best.

Postoperative atelectasis

Like the associated cough, the workup is usually nonproductive.

Deep breathing/incentive spirometry—equally effective

Postoperative pneumonia takes up to 5 days to manifest.

Productive cough, fever/chills, increased WBC count

Radiograph: pulmonary infiltrates

Smoking cessation improves outcomes

Patients should stop 6–8 weeks preoperatively.

Nicotine supplements do no harm to wound.

Fewer pulmonary complications

•

Smokers have six times more pulmonary complications.

Fewer wound healing issues and wound infections

•

Lower nonunion rate

•

Shoulder, neck, and thoracic pain in smokers

Prompts careful evaluation of lung fields

Superior sulcus tumor (Pancoast tumor)

Intrinsic atrophy of hand—C8–T1

28
Q

Describe ARDS:

A

Pulmonary failure due to edema (see Fig. 1.56A)

Pathophysiology

Complement pathway activated

Increased pulmonary capillary permeability

Intravascular fluid floods alveoli

Results

Hypoxia, pulmonary HTN

Right heart failure

50% mortality

Etiology

Blunt chest trauma, aspiration, pneumonia, sepsis

Shock, burns, smoke inhalation, near drowning

Orthopaedic: Long-bone trauma

Clinical symptoms

Tachypnea, dyspnea, hypoxia, decreased lung compliance

Pao2/fio2 ratio below 200

Imaging:

Radiographs: diffuse bilateral infiltrates, “snowstorm”

CT: ground glass appearance

Treatment: Aggressive supportive care

Prompt diagnosis and treatment of musculoskeletal infections:Prompt treatment of long-bone fractures

Ventilation with positive end-expiratory pressure (PEEP)

100% O2

29
Q

Describe Fat Emboli Syndrome:

A

Petechial rash: fat to skin

Neurologic symptoms: fat to brain

Mental status changes: confusion, stupor

Rigidity, convulsions, coma

Pulmonary collapse: fat showers lung

ARDS: hypoxia, tachypnea, dyspnea

Associated with long-bone fractures

30
Q

Characterize the common blood disoders as it relates to surgery:

A

Common inherited bleeding disorders:

Vonwillebrands disease AD (Vonwillebrands factor)

Hemophilia Ax-linked recessive

Hemophilia B. Christmas

Von Willebrand disease: autosomal dominant

Most common genetic coagulation disorder

Von Willebrand factor dysfunction

Binds platelets to endothelium

Carrier for factor VIII

Treatment: desmopressin

Hemophilia A (VIII): X-linked recessive

Hemophilia B (IX) Christmas disease: X-linked recessive

31
Q

List some medications that should be stopped prior to surgery:

A

Platelet-inhibitor drugs (aspirin, clopidogrel, prasugrel, NSAIDs)

Drugs that cause thrombocytopenia

Penicillin, quinine, heparin, LMWH

Anticoagulants (see earlier discussion on DVT)

Supplements

Fish oil, omega-3 fatty acids, vitamin E

Garlic, ginger, Ginkgo biloba

32
Q

Review Tourniquet technique

A

Tourniquets: tissue effect relates to time and pressure

Used no longer than 2 hours

Time to restoration of equilibrium

5 minutes after 90 minutes of use

15 minutes after 3 hours

Prolonged use can cause tissue damage.

Nerve damage compressive (not ischemic)

Electromyography: subclinical abnormalities in 70% with routine use

Slight increase in pain

Wider tourniquets distribute forces

Pad underneath prevents skin blisters in TKA

•

Lowest pressure needed for effect should be used

100–150 mm Hg above systolic BP

200 mm Hg upper extremity

250 mm Hg lower extremity

33
Q

Ways to manage surgical bleeding:

A

Tranexamic acid

Synthetic lysine analogue; acts on fibrinolytic system

Competitive inhibitor of plasminogen activation

Reduces blood loss with no increase in DVT.

Temperature

Mild hypothermia increases bleeding time and blood loss.

•

Intraoperative “cell saver” may be cost-effective if:

About 1000 mL of blood loss is expected

Recovery of 1 or more unit of blood is anticipated.

Techniques not yet found to be effective or cost-effective

Bipolar sealant, topical sealants, autologous donation

Reinfusion systems, routine transfusions over 8 g/dL Hb

Preoperative techniques to address anemia

Oral iron 30–45 days preoperatively

Vitamin C increases iron absorbtion

Folate and vitamin B12 deficiency also a source of anemia

Erythropoietin if preoperative Hb below 13

34
Q

Review the risks and benefits of blood transfusion

A

Transfusions

•

Ratio of 1:1:1 blood product resuscitation is superior to saline fluid

•

Preoperative Hb most significant predictor of need

•

Various guidelines for when to transfuse

•

Hb less than 6 g/dL: transfusion

•

Hb 7–8 g/dL: transfusion of postoperative patients

•

Hb 8–10 g/dL: transfusion of symptomatic patients

•

Restrictive transfusion strategies

•

Lower 30-day mortality trend

•

Lower infection risk trend

•

Greatest benefits to orthopaedic patients

•

No difference in functional recovery

□

Transfusions risks

•

Leading risk: transfusion of wrong blood to patient

•

Occurs in 1 in 10,000 to 1 in 20,000 RBC units transfused

•

Transfusion reactions

Febrile nonhemolytic transfusion reaction

Most common

1–6 hours post-transfusion

From leukocyte cytokines released from stored cells

Leukoreduction decreases incidence

Acute hemolytic transfusion reaction

Medical emergency

ABO incompatibility

IgM anti-A and anti-B, which fix complement

Rapid intravascular hemolysis

Classic triad: fever, flank pain, red/brown urine (rare)

Can cause disseminated intravascular coagulation (DIC), shock, and acute renal failure (ARF) due to acute tubular necrosis (ATN)

Positive direct antiglobulin (Coombs) test result

Delayed hemolytic transfusion reactions

Reexposure to previous antigen (i.e., Rh or Kidd)

History of pregnancy, prior transfusion, transplantation

3–30 days post-transfusion

Anemia, mild elevation of unconjugated bilirubin, spherocytosis

Anaphylactic reactions: about 1 in 20,000

Rapid hypotension, angioedema

Shock, respiratory distress

Frequently involve anti-IgA and IgE antibodies

Treatment: cessation of transfusions, ABCs of resuscitation, epinephrine

Urticarial reactions: about 1%–3%

Mast cell/basophils release of histamine—hives

Infectious risks

Bacterial: 0.2 per million packed red blood cell (PRBC) units transfused

Gram-positive organisms

Cryophilic organisms: Yersinia, Pseudomonas

HTLV—approximately 1 in 2 million

HIV—approximately 1 in 2 million

Hepatitis C—approximately 1 in 2 million

Hepatitis B—approximately 1 in 250,000

35
Q

Review the Liver issues with surgery:

A

Liver failure: critical for producing proteins and metabolizing toxins

•

Laboratory findings

•

Increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin

•

INR above 1.5, low platelets (<150,000 cells/μL)

•

Acute—most commonly viral and drug induced

•

Acetaminophen—number one cause in United States

•

Other toxins: alcohol, occupational, mushrooms

•

Viral hepatitis

•

Chronic—cirrhosis is end-stage fibrosis of liver

•

Common: hepatitis (B, C), alcoholism, hemochromatosis

•

Classifications can be helpful to estimate risks

•

Child classification—most widely used

•

Based on laboratory results and physical examination

•

Model for End-Stage Liver Disease (MELD) score (http://www.mayoclinic.org/medical-professionals/model-end-stage-liver-disease/meld-model)

•

Formula based on bilirubin, INR, creatinine

•

Studies highlight mortality at 90 days relative to MELD score

•

<9: about 2% mortality

•

10–19: about 6% mortality

•

20–29: about 20% mortality

•

30–39: about 53% mortality

•

>40: about 71% mortality

•

Complication rates from surgery are extremely high.

•

In patients undergoing arthroplasty, MELD score above 10 predicted

•

Three times the complication rate

•

Four times the rate death

36
Q

What is Ogilvee’s syndrome?

A

Large bowel dilation

•

Abdominal distension the prominent symptom

•

Colonic perforation should be avoided.

•

Risk factors

•

Elderly or male patient

•

Previous bowel surgery

•

Diabetes, hypothyroidism

•

Electrolyte disorders

Radiographic findings

Distended transverse and descending colon and cecum (see Fig. 1.58C)

Colonic diameter more than 10 cm risks perforation.

Treatment

Nothing by mouth status

Neostigmine

Colonic decompression

37
Q

Review pseudomembraneous collitis

A

Most common antibiotic-associated colitis

Change in colon flora favors Clostridium difficile

Makes enterotoxin-A and cytotoxin-B

Many antibiotics

Clindamycin, fluoroquinolones

Penicillins and cephalosporins

Can become severe fulminant colitis

Toxic megacolon and perforations

•

Risk factors

Elderly hospitalized patient

Severe illness

Antibiotic use

Proton pump inhibitor use

•

Diagnosis

Watery diarrhea with fever

Leukocytosis, lower abdominal pain

Laboratory findings

WBC count more than 15,000 cells/μL

Stool specimen should be tested for C. difficile toxin

PCR or ELISA

KUB (kidney, ureter, bladder) (plain abdominal) radiograph

Toxic megacolon: greater than 7 cm

Thumbprinting (see Fig. 1.58D)

•

Treatment

Oral metronidazole

Oral vancomycin (IV will not work)

Fidaxomicin

Colectomy if unresponsive and severe

Megacolon, WBC count more than 20,000 cells/μL

38
Q

What are the surgical considerations for obstructive sleep apnea?

A

Intermittent hypercapnia and hypoxia

Decreased CO2-induced respiratory drive

Extreme sensitivity to opioids

Leads to

•

Pulmonary HTN

Cardiac arrhythmias

GERD (reflux) directly related to BMI

Delayed gastric emptying

Increased risks for aspiration/intubation

Higher risk for complications (2–4 times greater)

Respiratory failure, ICU transfers, increased length of stay

Increased postoperative O2 desaturation

Increased intubation, aspiration pneumonia, ARDS

Increased MI, arrhythmias (atrial fibrillation)

Screening tools: STOP-BANG (Fig. 1.59)

  • Snoring, tired, observed apnea, pressure (HTN)
  • BMI over 35, age older than 50 years, neck

circumference larger than 40 cm, gender male

Five or more factors present—high risk of

severe OSA

Best practices

Initiation or continuation of CPAP use

More than 2 weeks of preoperative CPAP

improved HTN, O2 saturation, apneic events

Pulmonary HTN: in 20%–40% of patients with

OSA

Preoperative serum bicarbonate predicts

hypoxia in OSA

Chronic respiratory acidosis

Site of service (American Society of Anesthesiology consensus statement)

Ambulatory surgery under local/regional—lower

risk

Avoid procedures requiring opioids—greater

risk

Comorbid conditions must be optimized for outpatient surgery. HTN, arrhythmias, CHF, cardiovascular disease, and metabolic syndrome.

Metabolic syndrome = obesity, hypertension, hypercholesterolemia, dyslipidemia, and insulin resistance

Avoidance of flat supine position; sitting position opens airway.

39
Q

Review Malignant hyperthermia:

A

Autosomal dominant genetic defect of T-tubule of sarcoplasmic reticulum

Ryanodine receptor defect (RYR1)

Dihydropyridine receptors (DHP)

Triggered by volatile anesthetics and succinylcholine

Creates an uncontrolled release of Ca2+

Sustained muscular contraction (masseter rigidity)

Increased end-tidal CO2

Earliest and most sensitive sign

Mixed respiratory and metabolic alkalosis

Hyperthermia is classic but occurs later.

•

Muscle damage

Myoglobin from rhabdomyolysis can cause ARF.

Elevated creatine kinase

Hyperkalemia can lead to ventricular arrhythmias.

Treatment with dantrolene

Decreases intracellular Ca2+

Stabilizes sarcoplasmic reticulum

Treatment of high serum potassium

Hydration

Cooling

40
Q

what are some radiation safety concerns for the orthopedic surgeon?

A

Should be considered for every fluoroscopic case

Increased radiation exposure associated with

–Imaging of larger body parts

–Positioning the extremity closer to the x-source

–Use of large C-arm rather than mini C-arm

Factors to decrease the amount of radiation exposure

–Minimizing exposure time

–Using collimation to manipulate the x-ray beam

–Use of protective shielding

–Maximizing the distance between the surgeon and

the radiation beam

–Utilizing mini C-arm whenever feasible (associated

with minimal radiation exposure)

–Surgeon control of the C-arm

41
Q

What are contraindications to MRI?

A

Contraindications

Pacemakers

Cerebral aneurysm clips

Shrapnel or hardware, in certain locations

42
Q

MRI Imaging Terminology

A
43
Q

Review of clinically relevant nuclear medicine studies:

A
44
Q

EMG interpretations:

A
45
Q

Key Highlights of NCS:

A

Evaluation of peripheral nerves

Nerve impulses stimulated and recorded by surface electrodes

Allows calculation of conduction velocity

Measures latency (time from stimulus onset to response) and response amplitude

Late responses (F wave, H reflex) allow evaluation of proximal lesions.

Impulse travels to the spinal cord and returns

Frank Review Course (34 decks)

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